Lesions of Orbitofrontal Cortex and Basolateral Amygdala Complex Disrupt Acquisition of Odor-Guided Discriminations and Reversals

  1. Geoffrey Schoenbaum1,
  2. Barry Setlow,
  3. Summer L. Nugent,
  4. Michael P. Saddoris, and
  5. Michela Gallagher
  1. Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, Maryland 21218, USA

Abstract

Recent work indicates that both orbitofrontal cortex (OFC) and the basolateral complex of the amygdala (ABL) are involved in processes by which cues are associated with predicted outcomes. To examine the respective roles of these structures in discrimination learning, rats with bilateral sham or neurotoxic lesions of either OFC or ABL were trained on a series of four 2-odor discrimination problems in a thirst-motivated go, no-go task. After acquisition of the series of odor problems, the rats were trained on serial reversals of the final odor problem. Performance on each problem was assessed by monitoring accuracy of choice behavior, and also by measuring latency to respond for fluid outcomes after odor sampling. During discrimination learning, rats in both lesioned groups had similar deficits, failing to show normal changes in response latency during learning, while at the same time exhibiting normal choice behavior relative to controls. Choice behavior was affected only during the reversal phase of training, in which OFC and ABL lesions produced distinctive deficits. Rats with ABL lesions were impaired on the first reversal (S1−/S2+), but were unimpaired at acquiring a reversal back to the original odor-outcome contigencies (S1+/S2−), whereas rats with OFC lesions were impaired on both types of reversals. These findings suggest that OFC and ABL serve partially overlapping roles in the use of incentive information that supports normal discrimination performance.

Footnotes

  • 1 Corresponding author.

  • E-MAIL schoenbg{at}jhu.edu; FAX (410) 516-6205.

  • Article and publication are at http://www.learnmem.org/cgi/doi/10.1101/lm.55203.

    • Received August 27, 2002.
    • Accepted December 5, 2002.
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